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Roussel Edouard Brasse-Lagnel Carole Tuech Jean-Jacques Montialoux Helène Papet Eloise Tortajada Pauline Bekri Soumeya Schwarz Lilian 《World journal of surgery》2022,46(3):656-665
World Journal of Surgery - By inhibiting the growth of pathogenic bacteria and modulating the local intestinal immune system, probiotics may reduce bacterial translocation and systemic... 相似文献
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Lidove O Bekri S Goizet C Khau Van Kien A Aractingi S Knebelmann B Choukroun G Tsimaratos M Redonnet-Vernhet I Lacombe D Jaussaud R 《Presse medicale (Paris, France : 1983)》2007,36(7-8):1084-1097
Fabry disease is a rare and under-recognized disease associated with an altered X-linked gene controlling hydrolase alpha-galactosidase A activity. This mutation impairs the glycosphingolipid metabolism. A multisystemic disease with a highly variable clinical presentation, its principal symptom is acroparesthesia. Manifestations of Fabry disease occur mostly in hemizygous males but also in heterozygous females. Before enzyme replacement therapy was available, life expectancy was about 50 years in men and 70 years in women. Early diagnosis is essential to prevent irreversible organ damage. Diagnosis is based on an assay of alpha-galactosidase A activity in male patients and on genetic analysis in female patients. Prognosis is related principally to three complications: involvement of the central nervous system, kidneys, and heart. Management of Fabry patients should in all cases combine symptomatic therapy and regular clinical, laboratory and morphological follow-up by specialists in genetic metabolic diseases. Enzyme replacement therapy should be considered in all adult male patients and should probably begin early. In adult heterozygous female patients and in children, this treatment should be considered only for patients with severe pain, organ damage, or central nervous system, kidney, or heart involvement. After a proband is identified, a genealogical tree should be used to identify other affected members of the family. 相似文献
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Soumeya Abed Alisa Tubsuwan Porntip Chaichompoo In Hyun Park Alice Pailleret A?ssa Benyoucef Lucie Tosca Edouard De Dreuzy Anais Paulard Marine Granger-Locatelli Francis Relouzat Stéphane Prost Gerard Tachdjian Suthat Fucharoen George Q. Daley Emmanuel Payen Stany Chrétien Philippe Leboulch Le?la Maouche-Chrétien 《Haematologica》2015,100(10):e428-e431
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Etienne Berard Mirande Candito Bernard Diaine Jean-Yves Kurzenne Soumeya Bekri Pierre Chambon Roger Mariani 《Pediatric nephrology (Berlin, Germany)》1996,10(6):761-763
We report a hypertensive child with renal artery stenosis who exhibited increased urinary excretion of norepinephrine (NE)
and normetanephrine (NMN), while vanillylmandelic acid (VMA) excretion was within the normal range. The NMN values prompted
us to investigate the patient for pheochromocytoma; for this purpose, NE was determined by plasma catecholamine assays in
venous samples obtained by catheterization. The moderately increased NE levels could not be localized to any particular sampling
site. Arteriography demonstrated right renal artery abnormalities. Following right nephrectomy with preservation of the right
adrenal gland, arterial blood pressure returned to normal. The cause of increased NMN excretion without a concomitant rise
in VMA during hypertension is discussed.
Received May 23, 1995; received in revised form and accepted February 6, 1996 相似文献
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Soumeya Hema‐Ouangraoua Abdoul Aziz Maiga Matthew Cairns Issaka Zongo Nikiema Frdric Rakiswend Serge Yerbanga Boubou Tamboura Henry Badji Georgia Gore‐Langton Irene Kuepfer Halidou Tinto Issaka Sagara Alassane Dicko Samba O. Sow Daniel Chandrahoman Brian Greenwood Jean Bosco Ouedraogo 《Tropical medicine & international health : TM & IH》2019,24(12):1442-1454
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Brachemi S Mambole A Fakhouri F Mouthon L Guillevin L Lesavre P Halbwachs-Mecarelli L 《Journal of the American Society of Nephrology : JASN》2007,18(8):2330-2339
We investigated membrane proteinase 3 (mPR3) expression during TNF-alpha-induced adhesion of neutrophils in the presence of anti-PR3 antibodies, a situation occurring during anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated vasculitis. Three increasing levels of mPR3 expression were observed on the mPR3(+) neutrophil subset after stepwise cell activation. TNF-alpha activation without adhesion, TNF-alpha-induced adhesion, and adhesion in the presence of anti-PR3 mAb or human anti-PR3 ANCA resulted, respectively, in a two-, seven-, and 24-fold increase of mPR3 levels. In plasma, anti-PR3 antibodies poorly recognized suspended neutrophils, whereas they bound to mPR3 on adherent cells. mPR3 upregulation was also triggered by IL-8, formyl-methionyl-leucyl-phenylalanine (fMLP), and neutrophil adhesion to activated human umbilical vein endothelial cells. It involved beta2 integrins and Fcgamma receptor, because it was prevented by anti-CD18 antibodies and was not observed with anti-PR3 F(ab')(2). Furthermore, it was specific to anti-PR3 mAb, and no mPR3 upregulation was observed with anti-myeloperoxidase or anti-HLA-ABC mAb. Newly expressed mPR3 molecules, after TNF-induced adhesion, were mobilized from secretory vesicles (CD35(+)) and secondary granules (CD11b(+)). The adhesion- and antibody-dependent upregulations of mPR3 expression occurred with little azurophilic granule degranulation, no sign of apoptosis, and no further CD177 upregulation. In conclusion, this study describes an amplifying loop in polymorphonuclear neutrophil activation process, whereby ANCA are involved in the membrane expression of their own antigen during cell adhesion. This could explain the restriction of ANCA-associated vasculitis to small vessels, the main site of neutrophil adhesion. 相似文献
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El Ghazi F Desfeux A Brasse-Lagnel C Roux C Lesueur C Mazur D Remy-Jouet I Richard V Jégou S Laudenbach V Marret S Bekri S Prevot V Gonzalez BJ 《Neurobiology of disease》2012,45(3):871-886
In industrialized countries, cerebral palsy affects 2.5‰ of preterm and term infants. At a neurochemical level, the massive release of glutamate constitutes a major process leading to excitotoxicity and neonatal brain lesions. Previous studies, conducted in the laboratory, revealed that, in (δ/δ)VEGF(A) transgenic mice, glutamate-induced brain lesions are exacerbated suggesting that VEGF(A) could play a protective action against excitotoxicity. Using a model of cultured cortical brain slices, the aim of the study was to characterize the central effects of VEGF against glutamate-induced excitotoxicity in neonates. Exposure of brain slices to glutamate induced a strong increase of necrotic cell death in the deep cortical layer VI and a decrease of apoptotic death in superficial layers II-IV. When administered alone, a 6-h treatment with VEGF(A) had no effect on both apoptotic and necrotic deaths. In contrast, VEGF(A) abolished the glutamate-induced necrosis observed in layer VI. While MEK and PI3-K inhibitors had no effect on the protective action of VEGF(A), L-NAME, a pan inhibitor of NOS, abrogated the effect of VEGF(A) and exacerbated the excitotoxic action of glutamate. Calcimetry experiments performed on brain slices revealed that VEGF(A) reduced the massive calcium influx induced by glutamate in layer VI and this effect was blocked by L-NAME. Neuroprotective effect of VEGF(A) was also blocked by LNIO and NPLA, two inhibitors of constitutive NOS, while AGH, an iNOS inhibitor, had no effect. Nitrite measurements, electron paramagnetic resonance spectroscopy and immunohistochemistry indicated that glutamate was a potent inducer of NO production via activation of nNOS in the cortical layer VI. In vivo administration of nNOS siRNA promoted excitotoxicity and mimicked the effects of L-NAME, LNIO and NPLA. A short-term glutamate treatment increased nNOS Ser1412 phosphorylation, while a long-term exposure inhibited nNOS/NR2B protein-protein interactions. Altogether, these findings indicate that, in deep cortical layers of mice neonates, glutamate stimulates nNOS activity. Contrasting with mature brain, NO production induced by high concentrations of glutamate is neuroprotective and is required for the anti-necrotic effect of VEGF(A). 相似文献